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Effects of general anesthetics on visceral pain transmission in the spinal cord
Current evidence suggests an analgesic role for the spinal cord action of general anesthetics; however, the cellular population and intracellular mechanisms underlying anti-visceral pain by general anesthetics still remain unclear. It is known that visceral nociceptive signals are transmited via pos...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2008
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2584043/ https://www.ncbi.nlm.nih.gov/pubmed/18973669 http://dx.doi.org/10.1186/1744-8069-4-50 |
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author | Wang, Yun Wu, Jing Lin, Qing Nauta, HJ Yue, Yun Fang, Li |
author_facet | Wang, Yun Wu, Jing Lin, Qing Nauta, HJ Yue, Yun Fang, Li |
author_sort | Wang, Yun |
collection | PubMed |
description | Current evidence suggests an analgesic role for the spinal cord action of general anesthetics; however, the cellular population and intracellular mechanisms underlying anti-visceral pain by general anesthetics still remain unclear. It is known that visceral nociceptive signals are transmited via post-synaptic dorsal column (PSDC) and spinothalamic tract (STT) neuronal pathways and that the PSDC pathway plays a major role in visceral nociception. Animal studies report that persistent changes including nociception-associated molecular expression (e.g. neurokinin-1 (NK-1) receptors) and activation of signal transduction cascades (such as the protein kinase A [PKA]-c-AMP-responsive element binding [CREB] cascade)-in spinal PSDC neurons are observed following visceral pain stimulation. The clinical practice of interruption of the spinal PSDC pathway in patients with cancer pain further supports a role of this group of neurons in the development and maintenance of visceral pain. We propose the hypothesis that general anesthetics might affect critical molecular targets such as NK-1 and glutamate receptors, as well as intracellular signaling by CaM kinase II, protein kinase C (PKC), PKA, and MAP kinase cascades in PSDC neurons, which contribute to the neurotransmission of visceral pain signaling. This would help elucidate the mechanism of antivisceral nociception by general anesthetics at the cellular and molecular levels and aid in development of novel therapeutic strategies to improve clinical management of visceral pain. |
format | Text |
id | pubmed-2584043 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-25840432008-11-18 Effects of general anesthetics on visceral pain transmission in the spinal cord Wang, Yun Wu, Jing Lin, Qing Nauta, HJ Yue, Yun Fang, Li Mol Pain Review Current evidence suggests an analgesic role for the spinal cord action of general anesthetics; however, the cellular population and intracellular mechanisms underlying anti-visceral pain by general anesthetics still remain unclear. It is known that visceral nociceptive signals are transmited via post-synaptic dorsal column (PSDC) and spinothalamic tract (STT) neuronal pathways and that the PSDC pathway plays a major role in visceral nociception. Animal studies report that persistent changes including nociception-associated molecular expression (e.g. neurokinin-1 (NK-1) receptors) and activation of signal transduction cascades (such as the protein kinase A [PKA]-c-AMP-responsive element binding [CREB] cascade)-in spinal PSDC neurons are observed following visceral pain stimulation. The clinical practice of interruption of the spinal PSDC pathway in patients with cancer pain further supports a role of this group of neurons in the development and maintenance of visceral pain. We propose the hypothesis that general anesthetics might affect critical molecular targets such as NK-1 and glutamate receptors, as well as intracellular signaling by CaM kinase II, protein kinase C (PKC), PKA, and MAP kinase cascades in PSDC neurons, which contribute to the neurotransmission of visceral pain signaling. This would help elucidate the mechanism of antivisceral nociception by general anesthetics at the cellular and molecular levels and aid in development of novel therapeutic strategies to improve clinical management of visceral pain. BioMed Central 2008-10-30 /pmc/articles/PMC2584043/ /pubmed/18973669 http://dx.doi.org/10.1186/1744-8069-4-50 Text en Copyright © 2008 Wang et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Wang, Yun Wu, Jing Lin, Qing Nauta, HJ Yue, Yun Fang, Li Effects of general anesthetics on visceral pain transmission in the spinal cord |
title | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_full | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_fullStr | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_full_unstemmed | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_short | Effects of general anesthetics on visceral pain transmission in the spinal cord |
title_sort | effects of general anesthetics on visceral pain transmission in the spinal cord |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2584043/ https://www.ncbi.nlm.nih.gov/pubmed/18973669 http://dx.doi.org/10.1186/1744-8069-4-50 |
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